Disease Fact sheets 2

Question 1

infectious bronchitis etiology, significance

Answer 1

• Common and economically important
• Corona virus with numerous serotypes and often new variant strains

Question 2

IB disease

Answer 2

Young birds - inflammation of the upper respiratory tract particularly tracheal and bronchi. Affected birds appear chilled and huddled and have poor growth performance. Sometimes bronchiolar or tracheal plugs may cause gasping or asphyxiation.
> Some strains are nephrotropic and cause kidney swelling and nephritis.
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Mature hens - In older birds IBV infects the oviduct causing decreased egg production and poor quality eggs often with abnormal shells.

Question 3

IB treatment and prevention

Answer 3

• None but supportive. Secondary bacterial infections may develop.
• Vaccination of both breeder flocks and young birds.

Question 4

Infectious Laryngotracheitis (ILT) species, imortance, etiology

Answer 4

• Disease of chickens, pheasants, quail and other game birds. There is also a strain of Psittacine herpes virus that causes a similar disease in Amazon parrots.
• Uncommon but economically important.
• Herpes virus

Question 5

ILT disease, signs

Answer 5

• severe acute infection of the upper
  respiratory system including primary bronchi and trachea.
• The virus is epitheliotropic and causes necrosis and sloughing of respiratory epithelium.
• Affected cells often contain typical intranuclear inclusion bodies.
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  Affected birds are depressed, show severe respiratory signs and often cough mucus and blood. Oral and nasal discharges and conjunctivitis also occur.

Question 6

ILT treatment and prevention

Answer 6

Treatment: None but supportive.
Prevention: Vaccination of breeder flocks and commercial birds (eye drop technique).

Question 7

ILT spread

Answer 7

ILT is mostly spread by direct contact between infected and susceptible birds.
The disease can also be spread by manure, equipment, clothing, or bird
carcasses contaminated with the virus. In some cases, wind-borne
transmission or darkling beetles may play a role in the spread.
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Mixing of birds with different health status is a significant risk factor for the
introduction of ILT to a flock. Vaccinated birds should not be mixed with birds
of unknown vaccination status.

Question 8

ILT prevention measures

Answer 8

Mixing of birds with different health status is a significant risk factor for the introduction of ILT to a flock.
Vaccinated birds should not be mixed with birds of unknown vaccination status. In addition, new birds should be segregated and monitored for at least 30 days before introducing them to an existing flock.

New birds should always come from reputable suppliers that have strict biosecurity and disease controls practices in place, such as licensed brokers or dealers or registered hatcheries.

All-in/all-out procedures are recommended to
avoid mixing infected and susceptible birds and to ensure that all the birds are of equal health status.

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The disease is controlled through biosecurity, vaccination, and communication.

Biosecurity is critical to contain the disease through proper management of litter, cleaning and disinfection of facilities and stopping unnecessary visits by people.

Litter should be heat-treated at 38°C (100°F) for 100 hours prior to movement and, if possible, should not be moved for 8 weeks to help destroy the virus. Vaccines for ILT are available, including attenuated or recombinant vaccines.

Question 9

ILT disease course

Answer 9

It takes anywhere from 6 to 14 days from when the bird
becomes infected to when it shows clinical signs allowing for asymptomatic
spread during this time. Five to 100% of the flock may become sick and
0 to 20% of the flock may die.

Question 10

stressful events which can activate ILT

Answer 10

mixing of new birds,
sudden weather changes, transportation, vaccination for other diseases and illness.

Question 11

ILT prevention measures

Answer 11

Vaccination
* If your previous flock was infected or if you are in close proximity to an infected premises, it is recommended
that broiler chicks be vaccinated for ILT for two successive crops.
* If you are a producer in the FBCC biosecurity advisory area, discuss with your veterinarian about vaccinating
your flock for ILT
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Manure management
* Heat-treat litter at 38° C (100° F) for 100 hours prior to thorough cleanout and disinfection.
* When possible, wait for 8 weeks before manure is moved off the premises. On-site manure must be covered to
reduce spread. If manure must be moved, ensure the manure hauler is aware of ILT on your farmand they
employ appropriate biosecurity practices including securely covering manure in transit.

Question 12

MAREK’S Disease - species, significance, etiology

Answer 12

• chickens mostly, no turkeys
• common,
  > Virtually every commercial chicken is vaccinated at day of age in the hatchery or at 18 in ovo to prevent Marek’s disease.
  > Clinical Marek’s disease is very common in backyard and hobby flocks where vaccination is not usually done.
• Herpesvirus, 3 serotypes. serotype 1 is the pathogenic type

Question 13

Marek’s disease pathogenesis and signs

Answer 13

• transformation of T lymphocytes and commonly causes lymphoid tumors in the nervous system and other organs.
• nervous system affected > lameness, CNS signs
• neo-plastic lymphocytic infiltrates in nerves (often sciatic) or a non-suppurative encephalitis.
• infected birds often develop visceral tumours, any organ can be affected

Question 14

Marek’s treatment and prevention

Answer 14

There is no treatment for Marek’s disease.
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Marek’s disease is readily transmitted from bird to bird through feather dust and dander. The virus replicates in feather follicle epithelium and the bird likely sheds virus for life.
Prevention is through vaccination at day 18 of embryonation (in ovo) or at day of hatch. The specific type (strain) of vaccine used is dependent on the strains of Marek’s virus found in that area. Virtually every commercial chicken in North Amer- ica and many parts of the world are routinely vaccinated.
Good barn management and thorough barn clean outs help to reduce the amount of virus in the environmental and reduce challenge to newly placed chicks.

Question 15

necrotic enteritis - species, significance, etiology

Answer 15

• Species: Primarily a disease of commercial broiler chickens, but necrotic enteritis also occurs in turkeys, wild and domestic waterfowl.
• Status in Canada: Common in broiler chickens
• Etiology: Clostridium perfringens (types A and C)

Question 16

necrotic enteritis signs, pathogenesis

Answer 16

• mortality in broilers aged 2+ weeks, usually aged 3+, when switched from starter to grower ration
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• C. perfringens is a normal part of the intestinal bacterial flora.
• Any event that changes the normal motility of the intestinal tract may allow C. perfrin- gens to multiply.
• If anaerobic condi- tions and substrate for bacterial growth are correct, the proliferating bacteria produce powerful necrotizing alpha or beta toxins that are responsi- ble for the necrosis of the cells of the intestine.
• Feed changes, a switch from a high protein to a lower protein ration, feed high in wheat or fish meal, or concurrent infections with coccidia all predispose to this disease.
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• Affected birds are depressed, lethar- gic and often have diarrhea. More of- ten they are found dead.
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  The gross lesions are found along the mucosal surfaces of the small intes- tine. These can range from small ero- sions or ulcerated areas to extensive necrosis and formation of a fibrinonec- trotic diphtheritic membrane over the intestinal surface.
  Affected chickens are depressed, have ruffled feathers and diarrhea
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• severe necrosis if intestinal villi

Question 17

necrotic enteritis treatment

Answer 17

Flocks can be treated with a variety of antibiotics including penicillin, ampicillin, lincomycin or zinc bacitracin. If coccidia are a factor, the use of anticoccidial drugs may be helpful.

Question 18

necrotic enteritis prevention

Answer 18

Many producers use routine antimicrobial medication to prevent NE. These are generally targeted at specific times where the disease is predictable such as just prior to the change of ration at 3 weeks of age. Good anticoccidial programs are also important in reducing NE and certain anticoccidial drugs like the ionophores have some additional antibacterial effects. Because of the growing concern about antibiotic resistance, there is increasing pressure to prevent and
manage necrotic enteritis using other means. This includes coccidial vaccines, control of dietary ingredients like high wheat content that may predispose NE, good litter quality including keeping litter moisture content as low as possible, re- ducing bird densities to reduce bacterial load in the litter, and good barn ventila- tion. There is some indication that competitive exclusion using probiotics may have a beneficial effect.

Question 19

Spondylolisthesis etiology

Answer 19

Not fully known but likely a combination of genetics, rapid growth rates and conformation. If one were to examine all of the mortality of a broiler flock, a few birds with this lesion would be identified.

Question 20

Spondylolisthesis pathogenesis, signs

Answer 20

Spondylolisthesis (commonly called Kinky Back in the in- dustry) is a deformity of the 6th thoracic vertebrae that causes varying degrees of spinal cord compression and leg paralysis.
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The 6th thoracic vertebrae is the one mobile joint in the nearly rigid backbone of the bird. This lesion always oc- curs at this location. The body of the 6th thoracic ver- tebra rotates on its axis re- sulting in partial subluxation of the vertebral body and compression of the spinal cord. Affected birds sit on their hocks and often flap their wings attempti ng to move forward, but in the process actually end up mov- ing backwards.

Question 21

spondylolisthesis Dx, Tx

Answer 21

Diagnosis
- Diagnosis is made by cutting the vertebral canal longitudinally and examining the area along T4-T6. The lesion is usually visible under gross examination. If one were to examine the spinal cord microscopically, there would be lesions as- sociated with pressure necrosis at the site of pinching.
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Treatment
- There is no treatment. Severely affected birds or those where normal growth is affected should be culled and removed from the flock.

Question 22

starve out cause, disease process, risks

Answer 22

• Inability of the young bird to locate the feed.
• Starve-outs occur during the first 5-10 days after the baby birds are placed on the farm
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  Management and environ- mental factors like heat and light and even substandard food and water quality may contribute to the disease.
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  Baby birds can live from nu- trients in the yolk sac for the first 5 days of life. However the longer it takes from hatching to reaching the farm, the higher the percent- age of birds that die of starve-out. The number of starve-outs increase mark- edly if birds are placed more than 72 hr after hatching. It is likely that birds initially dehy- drate a nd then lose their drive to find feed.
  Many will consume litter and digestive tracts are often full of bedding at necropsy
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Question 23

starve outs prevention

Answer 23

Starve-out is generally a management problem. Every effort should be made to start the birds as quickly as possible after hatching, making cer- tain the brooding temperatures are optimal, ensuring there are adequate feeders and palatable feed and fresh water. Extra feeding trays should be placed so that all birds have access to feed until they can locate the per- manent feed lines. Feed that is presented too large such as large pellets, or too fine and powdery, will inhibit feeding. Sore beaks from beak trim- ming may reduce the birds interest in eating.

Question 24

starve outs dx, tx

Answer 24

Diagnosis
- Diagnosis is made by examining birds and observing the typical changes and ruling out other infectious causes of disease.
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Treatment
- There is no treatment for individuals but any management factors should be quickly identified and corrected.

Question 25

Tibial dyschondroplasia etiology, disease

Answer 25

• Etiology: Not fully known but likely a combination of genetics, rapid growth rates and nutrition.
• defect in the growth plates of meat-type chickens, turkeys and ducks.
• avascular plug of abnormal cartilage in the growth zone of the long bones
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  The lesions is a result of retention and lack of differentiation of cartilage in the zones of pre-hypertrophy and hypertrophy combined with a failure of vascular channels to penetrate this abnormal cartilage.
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• Affected birds may be reluctant to move and have a stilted gait. If severe the growth zones of the bone may appear swollen and the legs may appear bowed.
• Most affected birds do not develop clinical signs

Question 26

Tibial dyschondroplasia dx, tx

Answer 26

Diagnosis
- Diagnosis is made by cutting the bone longitudinally and examining the growth zone. The lesion is usually visible using gross examination.
Treatment
- There is no treatment. Severely affected birds or those where normal growth is affected should be culled and removed from the flock.

Question 27

Valgus and Varus Deformation etiology, disease, prevention

Answer 27

Not fully known but likely a combination of genetics, rapid growth rates and nutrition. The incidence of this deviation can be reduced by slowing growth rates.
- long bone deformities, VVD is the most common leg deformity in broiler chickens.
- It may affect one or both legs. As the bird gains weight, more pressure is placed on the leg deformity making is worse. Eventually the gastrocnemius tendon (Achilles tendon) slips from its normal groove and results in a condition called “slipped tendon”.
- Affected birds may be reluctant to move and have grossly distorted legs. These birds can’t reach the feeders and slowly starve and dehydrate.

Question 28

What is proventricular dilatation syndrome?

Answer 28

The proventriculi are full of feed (up to 300-400g!) which
can lead to issues at processing including slowing of the
line speeds, lighter than expected eviscerated weights
and higher rates of carcass contamination. In some cases,
pendulous crops have also been reported. More recently,
there have been reports of higher on-farm mortality
attributed to sudden death. Many of these broilers have had
dilated feed-filled proventriculi

Question 29

What causes proventricular dilatation syndrome?

Answer 29

The cause of proventricular dilation has not been identified.
Currently it is called a “syndrome” and is thought to have a
multifactorial cause.
No breed or feed component (wheat vs corn-based diets) has been linked to the problem. Several processors
in multiple provinces processing different target weights of bird have been affected. Affected flocks have had
proper feed withdrawal prior to loading.
Proventricular dilation in chickens has been previously reported, linked to a variety of risk factors. Some of
the previously reported risk factors include: physiologic response to low fibre diets, biogenic amines
(histamine, cadaverine), copper sulfate, and mycotoxins

Question 30

avian reovirus system affected, type, disease caused

Answer 30

• GI
• most reavisruses dont cause disease, so isolating a reovirus doesnt mean it is the cause
• sigma c protein determines strain
• arthritis, runting-stunting

Question 31

viral arthritis signs

Answer 31

• 4-5 weeks old
• poor growth and uniformity
• lameness, tendon rupture
• culls 2-50%

Question 32

runting stunting syndrome signs

Answer 32

• uniformity issues by 2 weeks
• diarrhea 8-10d (malabsorptive)
• pale, growth retarded, abnormal feathers, femoral head fractures
• other pathogens also implicated besides reo

Question 33

reovirus transmission

Answer 33

horizontal - bird-bird, or environemtn
- via resp secretions, or feces
- contaminated litter + broken skin

vertical - oral, resp, skin, or egg transmission, then parent to progeny
- low rate of transmission

Question 34

reovirus management

Answer 34

biosecurity - clean and disinfect with adequate downtimes (14+d)
parent stock vaccination - less infection amongst breeders, and less vertical transmission, and maternal antibodies